Gerbils afford a good model for the study of lipid metabolism. When made inositol deficient, they develop an intestinal lipodystrophy. This is especially severe when saturated fats with a high proportion of lauric or myristic acids are fed in the inositol-free diets. Approximately two weeks are required for maximum fat accumulation to occur, and the fatty acid spectrum of the triglycerides is rich in fatty acids derived from the diet. Lipodystrophic animals given inositol in the diet or by injection begin to lose intestine mucosal lipid rapidly after a lag period of 3 to 12 hours. Return to normal intestine lipid levels occurs within 24 to 48 hours. This rapid tripglyceride removal phase affords a convenient initial system for studying the mecahnism by which inositol functions in ameliorating the lipodystrophy. The lag phase following inositol administration in vivo will also be examined for the earliest evidence of the response to insoitol. Both phases will be studied in intact animals, everted intestine segments, and subcellular preparations. Changes in lipid composition and enzyme activities will be monitored. The intestinal production of lipoproteins and chylomicron will be investigated during repletion. The significance of the decreased pH 9.0 lipase activity in the intestine due to inositol deficiency will be investigated. Dietary interactions on myo-inositol and cholesterol metabolism will be investigated by measuring the activity of regulatory enzymes in the metabolic pathway in selective tissues. The role of intestine in lipid metabolism of this species will be assessed under various nutritional conditions.